The Differences Between The pediatric and adult airways are important determinants of the anesthetic technique. Knowledge of normal developmental anatomy and physiologic function is required to understand and manage both the normal and the pathologic airways of infants and children ( ). Techniques and principles to assist in this management are reviewed in this chapter.

Developmental Anatomy of the Airway

The classic works by Negus, Eckenhoff, and Fink and Demarest shaped the foundation of our knowledge about the structure and function of the pediatric and adult airways. They suggested that there are five major anatomic differences between the neonatal and adult airways, which are outlined in this section, although recent studies suggest that not all of these long-held beliefs are valid. In addition, the relatively large head of an infant offsets the need to place anything under the head to achieve a proper “sniffing position.” Older children have airway features that represent a transition between the neonatal and adult anatomy.

Tongue

It is generally held that the tongue of the neonate and infant is relatively large in proportion to the rest of the oral cavity and therefore more easily obstructs the airway, especially in the neonate. However, magnetic resonance imaging (MRI) studies demonstrated that in children 1 to 11 years of age, there is proportional growth of the tongue and other soft tissues in relation to the bony structures of the oral cavity although that study did not examine neonates and infants (who are 1-12 months of age). The contribution of the tongue to upper airway obstruction with sedation or induction of anesthesia is relatively minor; much of the obstruction in older children is more likely attributable to the collapse of the nasopharynx and epiglottis, although the tongue may still contribute to obstruction in all age groups.

Position of the Larynx

The larynx in the infant is more cephalad than in the adult, classically described at the level of C3-4 in the former compared with C4-5 in the latter ( Fig. 14.1 ). MRI and computed tomography (CT) have confirmed the more cephalad position of the larynx in children and demonstrated that the hyoid bone is at the level of C2-3 in infants and children up to 2 years of age. Consequently, the distances between the tongue, hyoid bone, epiglottis, and roof of the mouth in infants are less than those in older children or adults.

FIGURE 14.1, In a preterm Infant, the larynx is located at the middle of the third cervical vertebra (C3); in a full-term infant, it is at the C3-4 interspace; and in an adult, it is at the C4-5 interspace.

The proximity of the tongue base to the more superior larynx also makes visualization of laryngeal structures more difficult because it produces a more acute angle between the plane of the tongue and the plane of the glottic opening. It is for this reason that a straight laryngoscope blade, which lifts the tongue from the field of view during laryngoscopy, facilitates visualization of an infant's larynx. This anatomic relationship is further complicated in certain conditions such as the Treacher Collins anomaly and other syndromes associated with mandibular and midfacial hypoplasia that make direct visualization of the glottis difficult and sometimes impossible with direct laryngoscopy ( Fig. 14.2 ). The reason for this difficulty is that with mandibular and midfacial hypoplasia, the base of the tongue is positioned more caudally (known as glossoptosis), in closer proximity to the laryngeal inlet than normal. The result is a more acute angle between the plane of the tongue and the plane of the laryngeal inlet (often 90 degrees) ( Fig. 14.3 ). In this situation, conventional rigid laryngoscopy provides excellent visualization of the esophageal inlet rather than the laryngeal inlet, necessitating the use of special equipment or special techniques to intubate the trachea.

FIGURE 14.2, Three-dimensional reconstruction of a child with the Treacher Collins anomaly demonstrates the retrognathic and more posterior position of the mandible, the midfacial hypoplasia, and the closer proximity and exaggerated angle between the base of the tongue and the laryngeal inlet (almost 90 degrees), which makes direct visualization of the larynx difficult.

FIGURE 14.3, The larynx in children with mandibular hypoplasia is located more posteriorly than in children with normal anatomy. A, Lateral radiograph of the upper airway including the base of the skull and cervical spine of a normal 7-year-old child; the arrows denote the posterior border of the ramus of the mandible and the anterior border of the second cervical vertebra. B, Diagrammatic representation of the normal anatomy in A . C, The same radiographic projection in a 6-year-old child with Treacher Collins syndrome; the arrows again denote the posterior border of the ramus of the mandible and the anterior margin of the second cervical vertebra. D, Diagrammatic representation of the anatomy in C . Notice the significantly smaller space between the ramus of the mandible and the second cervical vertebra, compared with the normal anatomy; the anterior margin of the first cervical vertebra overlaps the posterior margin of the mandible. This extreme posterior location of the tongue and larynx makes direct visualization of the laryngeal inlet almost impossible in many children with this anomaly because of the acute angulation between the base of the tongue and the laryngeal inlet.

Epiglottis

The epiglottis in the infant is narrow, omega shaped, and angled away from the axis of the trachea, which contrasts with that in the adult, which is flat and broad, and its axis is parallel to the trachea ( Figs. 14.4 and 14.5 ). This shape allows the epiglottis to approach the uvula during infant breastfeeding; separating breath from fluid and allowing respiration at the same time as swallowing. The shape of epiglottis makes it more difficult to directly lift in the neonate and infant with the tip of a laryngoscope blade.

FIGURE 14.4, Lateral neck xerogram (A) and schematic diagram (B) of the larynx in an adult. Notice the relatively thin, broad epiglottis, the axis of the epiglottis which is parallel to the trachea. The hyoid bone “hugs” the epiglottis; there is no subglottic narrowing. Also note how the vocal cords are perpendicular to the axis of the trachea.

FIGURE 14.5, Lateral neck xerogram (A) and schematic diagram (B) of an infant's larynx. Notice the angled epiglottis and the narrow cricoid cartilage. Also note that the vocal cords are angled with a higher attachment anteriorly than posteriorly compared with the perpendicular position of the vocal cords in adults.

Vocal Folds

The vocal folds (cords) in an infant are angled such that the anterior insertion is more caudad than the posterior insertion, whereas the axis of the folds in the adult is perpendicular to that of the trachea (compare Fig. 14.4A with Fig. 14.5A ). This anatomic feature alters the angle at which the tracheal tube approaches the laryngeal inlet and occasionally leads to difficulty with tracheal intubation, especially with the nasal approach. In the latter case, the tip of the endotracheal tube (ETT) may be held up at the anterior commissure of the vocal folds.

Subglottis

Classic teaching holds that the narrowest part of an infant's larynx is the cricoid cartilage; in an adult, it is the rima glottidis. This teaching was supported by an MRI and CT studies in young children (<2 years of age) who were sedated with oral medications and breathing spontaneously. In contrast, another study in children 2 months to 13 years of age undergoing MRI with propofol sedation and spontaneous respirations reported that the narrowest portions of the pediatric larynx were the glottic opening and the immediate sub–vocal cord level and that this finding did not change relative to the dimensions of the cricoid ring throughout childhood. These observations contradict the classic observations of autopsy specimens dating back to 1897 and other subsequent anatomic autopsy studies. The most likely reason for these apparent contradictory observations is that the more recent studies were conducted in spontaneously breathing children with variable portions of the respiratory cycle and that soft tissue collapse gives the appearance of a narrower airway above the cricoid cartilage. Nonetheless, when a relatively large-diameter tube is inserted into the glottic aperture, the tube readily passes through the distensible vocal cords but may meet resistance below the cords (e.g., the nondistensible cricoid ring region). Although these studies demonstrate in vivo dynamic, physiologic relationships, the cricoid cartilage is functionally the narrowest portion of the upper airway.

Growth of the subglottic airway occurs rapidly during the first 2 years of life; thereafter, growth of the airway is linear. The cricoid and thyroid cartilages reach adult proportions by 10 to 12 years of age, thus eliminating both the angulation of the vocal cords and the narrow subglottic area.

In adults, the rima glottidis is the narrowest part of the airway, and an ETT that traverses the glottis passes into the trachea without resistance. However, in about 70% of adult cadavers, the narrowest portion of the airway was identified in the subglottic region. The range in diameter for adult females is 10 to 16 mm, and for adult males it is 13 to 19 mm. The likely reason that ETTs pass easily through the rima glottidis into the trachea of an adult is that overall, the narrowest portion of the airway is still larger than the most commonly used ETT sizes. The apparent subglottic narrowing in adults is generally not evident unless there is the need to pass a larger-diameter ETT such as a double-lumen tube. In contrast, in a child, it is common for an ETT to pass easily through the vocal folds (glottic opening) but not through the subglottic region ( Fig. 14.6 ; see ). The larynx in both children and adults should be considered funnel-shaped, although this configuration is exaggerated and is of greater importance in infants and young children than in adults.

FIGURE 14.6, Configuration of the larynx of an adult (A) and an infant (B) . Notice that both larynxes are somewhat funnel shaped, but this shape is exaggerated in the infant and toddler. The adult laryngeal structures are of such size that most endotracheal tubes pass easily into the trachea. In infants and toddlers, it is common for the endotracheal tube (ETT) to pass easily through the vocal cords but to become snug at the level of the nondistensible cricoid cartilage. Concern for causing edema at this point resulted in the classic teaching that uncuffed ETTs should be used in young children (see text for more details). A, anterior; P, posterior.

The cricoid is the only complete ring of cartilage in the laryngotracheobronchial tree; as such it is nondistensible. Because the mucosa that lines the upper airway is loose-fitting pseudostratified columnar epithelium, pressure on the mucosa may cause reactive edema that encroaches on the diameter of the lumen. A tight-fitting ETT that compresses the tracheal mucosa at this level may cause inflammation and edema when it is removed, reducing the luminal diameter and increasing the airway resistance at the time of extubation (e.g., postextubation croup). Because the subglottic region in the infant is smaller than in the adult, the same degree of airway edema results in greater resistance in the infant. For example, assuming that the diameter of the cricoid ring in the infant is 4 mm and the diameter of the adult cricoid ring or trachea is 8 mm, 1 mm of edema circumferentially within the airway (i.e., reduction of the diameter of the airway by 2 mm) would decrease the cross-sectional area of the airway in the infant by approximately 75% (to 2 mm), whereas the area in the adult would decrease by only 44% (to 6 mm). Physiologically, because the resistance to airflow in the upper airway is turbulent, this reduction in diameter of the upper airway would increase the resistance to flow by the radius to the fifth power , or 32-fold, in the infant, compared with 5-fold in the adult. ( Fig. 14.7 ).

FIGURE 14.7, Relative effects of airway edema in an infant and an adult. The normal airways of an infant and an adult are presented on the left. Edematous airways display 1 mm of circumferential edema, reducing the diameter of the lumen by 2 mm. Notice that resistance to airflow is inversely proportional to the radius of the lumen to the fourth power for laminar flow (beyond the fifth bronchial division) and to the radius of the lumen to the fifth power for turbulent flow (from the mouth to the fourth bronchial division). The net result in an infant with a 4-mm diameter airway is a 75% reduction in cross-sectional area and a 16-fold increase in resistance to laminar airflow, compared with a 44% reduction in cross-sectional area and a 3-fold increased resistance in an adult with a similar 2-mm reduction in airway diameter. With turbulent airflow (upper airway), the resistance increases 32-fold in the infant but only 5-fold in the adult.

The Larynx

Understanding the anatomy and function of the larynx is critical to knowledgeable, safe, and successful airway management.

Anatomy

Structure

The larynx is composed of 1 bone (hyoid) and 11 cartilages (the single thyroid, cricoid, and epiglottic cartilages and the paired arytenoid, corniculate, cuneiform, and triticeal cartilages). These cartilages are suspended by ligaments from the base of the skull. The body of the cricoid cartilage articulates posteriorly with the inferior cornu of the thyroid cartilage. The paired triangular arytenoid cartilages rest on top of, and articulate with the superoposterior aspect of the cricoid cartilage. The arytenoid cartilages are protected by the thyroid cartilage ( Fig. 14.8 ). The triticeal cartilages are rounded nodules of cartilage, approximately the size of a pea in adults, located in the margins of the lateral thyrohyoid ligament.

FIGURE 14.8, Laryngeal cartilages. The natural positions of the laryngeal cartilages are presented on the left, with the individual cartilages separated on the right.

Tissue folds and muscles cover these cartilages. In contrast to adults, but comparable to most mammals, the cartilaginous glottis accounts for 60% to 75% of the length of the vocal folds in children younger than 2 years of age. Contraction of the intrinsic laryngeal muscles alters the position and configuration of these tissue folds, thus influencing laryngeal function during respiration, forced voluntary glottic closure (Valsalva maneuver), reflex laryngospasm, swallowing, and phonation ( Fig. 14.9 ).

FIGURE 14.9, Photograph (A) and schematic diagram (B) of the larynx of a premature infant.

The laryngeal tissue folds consist of the following:

  • Paired aryepiglottic folds extending from the epiglottis posteriorly to the superior surface of the arytenoids (the paired cuneiform and corniculate cartilages lie within for support and reinforcement, much like the metal stays in a shirt collar)

  • Paired vestibular folds (false vocal cords) extending from the thyroid cartilage posteriorly to the superior surface of the arytenoids

  • Paired vocal folds (true vocal cords) extending from the posterior surface of the thyroid plate to the anterior projection or vocal process of the arytenoids

  • A single interarytenoid fold (composed of the interarytenoid muscle covered by tissue) bridging the arytenoid cartilages

  • A single thyrohyoid fold extending from the hyoid bone to the thyroid cartilage

Histology

The highly vascular mucosa of the mouth is continuous with that of the larynx and trachea. This mucosa consists of squamous, stratified, and pseudostratified ciliated epithelium. The vocal cords are covered with stratified epithelium. The mucosa and submucosa are rich in lymphatic vessels and seromucous-secreting glands, which lubricate the laryngeal folds. The submucosa consists of loose fibrous stroma; therefore the mucosa is loosely adherent to the underlying structures in most areas. However, the submucosa is scant on the laryngeal surface of the epiglottis and the vocal cords, so the mucosa is tightly adherent in these areas. Most inflammatory processes of the airway above the level of the vocal cords are limited by the barrier formed by the firm adherence of the mucosa to the vocal cords. For example, the inflammation of epiglottitis is usually limited to the supraglottic structures, and the loosely adherent mucosa explains the ease with which localized swelling occurs (see Figs. 33.22 and 33.23 ). In a similar manner, an inflammatory process of the subglottic region (laryngotracheobronchitis [croup]) results in significant subglottic edema in the loosely adherent mucosa of the airway below the vocal cords, but it does not usually spread above the level of the vocal cords (see Fig. 33.21C ).

Sensory and Motor Innervation

Two branches of the vagus nerve, the recurrent laryngeal and the superior laryngeal nerves, supply both sensory and motor innervation to the larynx. The superior laryngeal nerve has two branches: the internal branch, which provides sensory innervation to the supraglottic region, and the external branch, which supplies motor innervation to the cricothyroid muscle. The recurrent laryngeal nerve provides sensory innervation to the subglottic larynx and motor innervation to all other laryngeal muscles. Local anesthetic agents injected to block the superior laryngeal nerve result in anesthesia of the supraglottic region down to the inferior margin of the epiglottis and motor blockade of the cricothyroid muscle, which causes relaxation of the vocal cords. Translaryngeal injection of local anesthetic through the cricothyroid membrane or a specific recurrent laryngeal nerve block is required for infraglottic and tracheal anesthesia.

Blood Supply

Laryngeal branches of the superior and inferior thyroid arteries provide the blood supply to the larynx. The recurrent laryngeal nerve and artery lie in close proximity to each other, which accounts for the occasional vocal cord paresis after attempts to control bleeding during thyroidectomy.

Function

Inspiration

During inspiration, the larynx is pulled caudad by the negative intrathoracic pressure generated by the descent of the diaphragm and contraction of the intercostal muscles. Thus, the larynx is stretched longitudinally, increasing the distance between the aryepiglottic and vestibular folds as well as between the vestibular and vocal folds. When the intrinsic muscles within the larynx contract, the arytenoids move laterally and posteriorly (rocking backward and rotating laterally), increasing the interarytenoid distance and separating as well as stretching the paired aryepiglottic, vestibular, and vocal folds. Overall, inspiration enlarges the laryngeal inlet, both longitudinally (like opening a telescope) and laterally, allowing the passage of greater quantities of air through the airway per unit time.

Expiration

At the end of expiration, the larynx reverts to its resting position, with longitudinal shortening of the distance between the aryepiglottic, vestibular, and vocal folds (like closing of a telescope). The arytenoids return simultaneously to their resting position by rotating medially and rocking forward, thus decreasing the interarytenoid distance and reducing the tension on the paired aryepiglottic, vestibular, and vocal folds and causing them to thicken.

Forced Glottic Closure and Laryngospasm

Glottic closure during forced expiration (forced glottic closure or Valsalva maneuver) is voluntary laryngeal closure and is physiologically similar to involuntary laryngeal closure (laryngospasm). Forced glottic closure occurs at several levels. Contraction of the intrinsic laryngeal muscles results in (1) marked reduction in the interarytenoid distance; (2) anterior rocking and medial movement of the arytenoids that causes apposition of the paired vocal, vestibular, and aryepiglottic folds; (3) longitudinal shortening of the larynx that obliterates the space between the aryepiglottic, vestibular, and vocal folds (like complete closing of a telescope). Contraction of an extrinsic laryngeal muscle, the thyrohyoid, pulls the hyoid bone caudad and the thyroid cartilage upward (cephalad), leading to further closure.

Closure of the larynx during laryngospasm is similar to, but not identical to that described for voluntary forced glottic closure. There are two important differences. First, laryngospasm is accompanied by an inspiratory effort, which longitudinally separates the vocal from the vestibular folds. Second, in contrast to forced glottic closure, neither the thyroarytenoid muscle (an intrinsic muscle of the larynx) nor the thyrohyoid muscle contract; thus, apposition of the aryepiglottic folds and median thyrohyoid folds is minimal. These two differences allow the upper portion of the larynx to be left partially open during mild laryngospasm, resulting in the hallmark high-pitched inspiratory stridor (see ). Anterior and upward displacement of the mandible (jaw thrust applied at the condyle of the ascending ramus of the mandible) longitudinally separates the base of the tongue, the epiglottis, and the aryepiglottic folds from the vocal folds, helping to relieve laryngospasm.

Swallowing

Glottic closure during swallowing is also similar to that which occurs during forced closure of the glottis. Protection of the glottic opening is achieved primarily by apposition of the laryngeal folds and secondarily by upward (cephalad) movement of the larynx. The upward movement of the larynx brings the thyroid cartilage closer to the hyoid bone, resulting in folding of the epiglottis over the glottic opening. With loss of consciousness or deep sedation, the normal protective mechanism of the larynx may be lost or obtunded, thus predisposing to pulmonary aspiration of pharyngeal contents.

Phonation

Phonation is accomplished by alteration of the angle between the thyroid and cricoid cartilages (the cricothyroid angle) and by medial movement of the arytenoids during expiration. These movements result in fine alterations in vocal fold tension during movement of air, causing vibration of the vocal folds. Lesions or malfunctions of the vocal folds (e.g., inflammation, papilloma, paresis) therefore affect phonation. Phonation is the only laryngeal function that alters the cricothyroid angle. Therefore, despite significant airway obstruction during inspiration, it may still be possible to phonate.

Physiology of the Respiratory System

Obligate Nasal Breathing

Infants are considered obligate nasal breathers. Obstruction of their anterior or posterior nares (nasal congestion, stenosis, choanal atresia) can cause asphyxia. Immaturity of coordination between respiratory efforts and oropharyngeal motor and sensory input accounts in part for obligate nasal breathing. Furthermore, because the larynx is more cephalad in the neck of an infant and oropharyngeal structures are closer together, the tongue rests against the roof of the mouth during quiet respiration, resulting in oral airway obstruction. Multiple sites of pharyngeal airway obstruction may also contribute to airway obstruction when the infant attempts to breathe against a partially obstructed upper airway or with relaxation of upper airway muscle tone after sedation or induction of anesthesia.

The ability to coordinate breathing and swallowing improves as the infant matures. The larynx enlarges and moves more caudad in the neck as the cervical spine lengthens and the infant begins to breathe adequately through the mouth. This matures by age 3 to 5 months. The ability to breathe through the mouth when the nares are obstructed is age dependent: 8% of preterm infants of 31 to 32 weeks postconception age were able to breathe through the mouth in response to nasal occlusion compared with 28% of more mature preterm infants of 35 to 36 weeks postconception age ; approximately 40% of full-term infants can switch from nasal to oral breathing. However, the ability of premature neonates to breathe through the mouth may not be as poor as these early reports suggested. Slow and fast nasal occlusion applied to 17 healthy preterm infants (gestational age, 32 ± 1 weeks; postnatal age, 12 ± 2 days) led to a switch from nasal to oral breathing. These improved results were attributed to the more extended observation period (>15 seconds) in the later study. The presence of a nasogastric tube may also affect the infant's breathing if the “unobstructed” nasal passage has an existing underlying obstruction.

Tracheal and Bronchial Function

Tracheal and bronchial diameters are a function of elasticity and of distending or compressive forces ( Fig. 14.10 ). The larynx, trachea, and bronchi in the infant are quite compliant compared with those in the adult and therefore are more subject to distention and compression forces. The intrathoracic trachea is subject to stresses that are different from those in the extrathoracic portion. During expiration, intrathoracic pressure remains slightly negative, maintaining patency of the intrathoracic trachea and bronchi (see Fig. 14.10B ). During inspiration, a greater negative intrathoracic pressure dilates and stretches the intrathoracic trachea and bronchi. The extrathoracic trachea at the thoracic inlet is slightly narrowed by dynamic compression that results from the differential between intratracheal and atmospheric pressures. However, the cartilages of the trachea, along with the muscles and soft tissues of the neck, maintain patency of the airway (see Fig. 14.10A ).

FIGURE 14.10, A, With descent of the diaphragm and contraction of the intercostal muscles, a greater negative intrathoracic pressure relative to intraluminal and atmospheric pressure is developed. The net result is longitudinal stretching of the larynx and trachea, dilatation of the intrathoracic trachea and bronchi, movement of air into the lungs, and some dynamic collapse of the extrathoracic trachea ( arrow ) . The dynamic collapse is due to the highly compliant trachea and the negative intraluminal pressure in relation to atmospheric pressure. B, The normal sequence of events at end-expiration is a slight negative intrapleural pressure stenting the airways open. In infants, the highly compliant chest does not provide the support required; therefore airway closure occurs with each breath. Intraluminal pressures are slightly positive in relation to atmospheric pressure, with the result that air is forced out of the lungs. C, Obstructed extrathoracic airway. Notice the severe dynamic collapse of the extrathoracic trachea below the level of obstruction. This collapse is greatest at the thoracic inlet, where the largest pressure gradient exists between negative intratracheal pressure and atmospheric pressure ( arrow ). (Extrathoracic upper airway obstruction is characterized by inspiratory stridor.) D, Obstructed intrathoracic trachea or airways. Notice that breathing against an obstructed lower airway (e.g., bronchiolitis, asthma) results in greater positive intrathoracic pressures, with dynamic collapse of the intrathoracic airways (prolonged expiration or wheezing [ arrows ]).

Obstruction of the extrathoracic upper airway that can occur with epiglottitis, laryngotracheobronchitis, or an extrathoracic foreign body alters normal airway dynamics. Inspiration against an obstruction results in more negative intrathoracic pressure, further dilating the intrathoracic airways. Clinically, the net effect is a dynamic collapse of the extrathoracic trachea below the level of the obstruction. This collapse is maximal at the thoracic inlet, where the greatest pressure gradient exists between negative intratracheal and atmospheric pressures. As a result, inspiratory stridor is prominent (see Fig. 14.10C and ). With intrathoracic tracheal obstruction (e.g., foreign body, vascular ring) (see ), stridor may occur during both inspiration and expiration. In lower airway obstruction (e.g., asthma, bronchiolitis), significant intrathoracic tracheal and bronchial collapse may occur as a result of the prolonged expiratory phase and greatly increased positive extraluminal pressure (see Fig. 14.10D ). In addition, because the airways in children are very compliant, they may be more susceptible to closure during bronchial smooth muscle contraction (e.g., with reactive airway disease). Preterm and term infants may experience airway closure even during quiet respiration.

Avoiding dynamic airway collapse is particularly important. The very compliant trachea and bronchi of an infant or child are prone to collapse, particularly at the extremes of transluminal pressures that may occur when a child is crying vigorously. The susceptibility of a child to these dynamic forces on the airway is inversely related to age, with preterm infants being most susceptible and adults being least susceptible. For this reason, it is essential that children with airway obstruction remain calm. Skill and understanding are required on the parts of the parents, nursing staff, and physicians. Sedatives and opioids should be used with caution before insertion of an ETT, because they may depress or ablate the life-sustaining voluntary efforts to breathe, resulting in significant morbidity or mortality.

Work of Breathing

Work of breathing (WOB) may be defined as the product of pressure and volume. It may be analyzed by plotting transpulmonary pressure against tidal volume. The WOB per kilogram body weight is similar in infants and adults. However, the oxygen consumption of a full-term neonate (5–7 mL/kg per minute) is several times that of an adult (2-3 mL/kg per minute). This greater oxygen consumption (and greater carbon dioxide production) in infants accounts in part for their increased respiratory frequency compared with older children. In preterm infants, the oxygen consumption related to breathing is three times that in adults.

The location of airway resistance within the tracheobronchial tree differs between infants and adults. The nasal passages account for 25% of the total resistance to airflow in a neonate, compared with 60% in an adult. In infants, most resistance to airflow occurs in the bronchi and small airways. This results from the relatively smaller diameter of the airways and the greater compliance of the supporting structures of the trachea and bronchi. In particular, the soft cartilaginous chest wall of a neonate is very compliant; the ribs provide less support to maintain negative intrathoracic pressure. This lack of negative intrathoracic pressure combined with the increased compliance of the bronchi can lead to functional airway closure with every breath. In infants and children, therefore, small-airway resistance accounts for most of the WOB, whereas in adults, the nasal passages provide the major proportion of flow resistance.

In the presence of increased airway resistance or decreased lung compliance, an increased transpulmonary pressure is required to produce a given tidal volume, and therefore the WOB is increased. Any change in the airway that increases the WOB may lead to respiratory failure. Recall that the WOB (resistance to air flow) is inversely proportional to the fourth power of the radius of the lumen during laminar flow (beyond the fifth bronchial division) and to the fifth power of the radius during turbulent flow (upper airway to the fifth bronchial division). Because the diameter of the airways in infants is smaller than in adults, pathologic narrowing of the airways in infants exerts a greater adverse effect on the WOB. Increase in the WOB may also occur with a long ETT of small diameter, an obstructed ETT, or a narrowed airway. All of these situations increase oxygen consumption, which in turn increases oxygen demand. The increased oxygen demand is initially addressed by an increase in respiratory rate, but the increased WOB may not be sustainable. The end result may be exhaustion, which leads to respiratory failure (CO 2 retention and hypoxemia) ( Fig. 4.9 ).

The difference in histology of the diaphragm and intercostal muscles of preterm and full-term infants compared with older children contributes to increased susceptibility of infants to respiratory fatigue or failure. Type I muscle fibers permit prolonged repetitive movement; for example, long-distance runners through repeated exercise increase the proportion of type I muscle fibers in their legs. The percentage of type I muscle fibers in the diaphragm and intercostal muscles increases with age (preterm infants < full-term infants < 2-year-old children) ( Fig. 14.11 ). Any condition that increases the WOB in preterm and full-term neonates may fatigue the respiratory muscles and precipitate respiratory failure more readily than in an adult.

FIGURE 14.11, Muscle fiber composition of the diaphragm and intercostal muscles related to age. Note that a preterm infant's diaphragm and intercostal muscles have fewer type I fibers compared with term newborns and older children. The data suggest a possible mechanism for early fatigue in preterm and term infants when the work of breathing is increased.

Airway Obstruction During Anesthesia

Airway obstruction during anesthesia or loss of consciousness appears to be most frequently related to loss of muscle tone in the pharyngeal and laryngeal structures rather than apposition of the tongue to the posterior pharyngeal wall. The progressive loss of tone with deepening anesthesia results in progressive airway obstruction primarily at the level of the soft palate and the epiglottis. In children, the pharyngeal airway space decreases in a dose-dependent manner with increasing concentrations of both sevoflurane and propofol anesthesia. This reduction in pharyngeal space has been observed mainly in the anteroposterior dimension. As the depth of propofol anesthesia in children increases, upper airway narrowing occurs throughout the entire upper airway but is most pronounced in the hypopharynx at the level of the epiglottis. Extension of the head at the atlantooccipital joint with anterior displacement of the cervical spine (sniffing position) improves hypopharyngeal airway patency but does not necessarily change the position of the tongue. This observation supports the concept that upper airway obstruction is not primarily caused by changes in tongue position but rather by collapse of the pharyngeal structures.

Pharyngeal airway obstruction also occurs during obstructive sleep apnea in children and adults. The sniffing position increases the cross-sectional area and decreases the closing pressure of both the retropalatal and the retroglossal space in anesthetized adults with obstructive sleep apnea. The application of continuous positive airway pressure (CPAP) is a common method to overcome such airway obstruction (see Figs. 33.10 and 33.11 ). During propofol anesthesia in children, CPAP works primarily by increasing the transverse dimension of the airway. This occurs despite the fact that anesthesia obstructs the airway mostly by narrowing the anteroposterior dimension. Chin lift and jaw thrust also improve airway patency in anesthetized children with adenotonsillar hypertrophy. Lateral positioning (also known as the “recovery or tonsillectomy position”) dramatically enhances the effects of these airway maneuvers ; lateral positioning alone improves airway dimensions. Compared with chin lift and CPAP, the jaw thrust maneuver is the most effective means to improve airway patency and ventilation in children undergoing adenotonsillectomy (see ).

Evaluation of the Airway

A history and physical examination with specific reference to the airway should be performed in all children who require sedation or anesthesia. In particular, a history of a congenital syndrome or physical findings of a congenital anomaly (e.g., microtia, which has been associated with difficult laryngoscopy) should alert the practitioner to the possibility of difficulties with airway management. In special situations, radiologic and laboratory studies are required to further evaluate and clarify a disorder revealed by the history and physical examination. Although many methods exist for evaluating and predicting the difficult airway in adults, no comparable methods have been forthcoming in children. Large neck circumference correlated with other issues, such as snoring, asthma, hypertension, and diabetes in children as well as adverse perioperative respiratory events, but not with difficult laryngoscopy. Routine evaluation of the airway in all children often sheds insight into the risk of a difficult airway. Characteristics that portend a difficult laryngoscopy and intubation include diagnosis of a specific syndrome associated with a difficult intubation (e.g., Treacher Collins syndrome), the inability to open the mouth (e.g., temporomandibular joint ankylosis, micrognathia Pierre Robin sequence or first arch syndrome), massive glossoptosis (e.g., Beckwith-Wiedemann syndrome), fused cervical spine (e.g., Klippel-Feil syndrome), or oropharyngeal space occupying lesions (e.g., cystic hygroma or glossopharyngeal tumors). For some syndromes, the airway improves with age (e.g., Pierre Robin sequence), whereas with others (e.g., Treacher Collins), the airway becomes progressively more difficult with age.

Clinical Evaluation

Medical History

The medical history (both present and past) should investigate the following signs and symptoms; a positive history should alert the practitioner to the potential problems noted in parentheses.

  • Presence of an upper respiratory tract infection (predisposition to coughing, laryngospasm, bronchospasm, and desaturation during anesthesia or to postintubation subglottic edema or postoperative desaturation)

  • Snoring, noisy breathing, obesity (adenoidal hypertrophy, upper airway obstruction, obstructive sleep apnea, pulmonary hypertension)

  • Presence and nature of cough (“croupy” cough may indicate subglottic stenosis or previous tracheoesophageal fistula repair; productive cough may indicate bronchitis or pneumonia; chronicity affects the differential diagnosis [e.g., the sudden onset of a persistent cough may indicate foreign-body aspiration; a night cough may indicate tracheal compression from a thoracic mass])

  • Past episodes of croup (postintubation croup, subglottic stenosis)

  • Inspiratory stridor, usually high-pitched (subglottic narrowing [see ], laryngomalacia [see ], macroglossia, laryngeal web [ ], extrathoracic foreign body or extrathoracic tracheal compression)

  • Hoarse voice (laryngitis, vocal cord palsy, papillomatosis [see ], granuloma [see ])

  • Asthma and bronchodilator therapy (bronchospasm)

  • Repeated pneumonias (incompetent larynx with aspiration, gastroesophageal reflux, cystic fibrosis, bronchiectasis, residual tracheoesophageal fistula, pulmonary sequestration, immune suppression, congenital heart disease)

  • History of foreign-body aspiration (increased airway reactivity, airway obstruction, impaired neurologic function)

  • History of aspiration (laryngeal edema [ ], laryngeal cleft)

  • Previous anesthetic problems, particularly related to the airway (difficult intubation, difficulty with mask ventilation, failed or problematic extubation)

  • Atopy, allergy (increased airway reactivity)

  • History of smoking by primary caregivers (increased airway resistance, increased propensity to desaturation)

  • History of a congenital syndrome (many are associated with difficult airways)

  • History of prematurity (subglottic stenosis, bronchopulmonary dysplasia, apnea, desaturation)

Physical Examination

The physical examination should include the following observations:

  • Facial expression

  • Presence or absence of nasal flaring

  • Presence or absence of mouth breathing

  • Color of mucous membranes

  • Presence or absence of retractions (suprasternal, intercostal, subcostal [see ])

  • Respiratory rate

  • Presence or absence of voice change

  • Mouth opening ( Fig. 14.12A )

    FIGURE 14.12, A, How far can a child open his or her mouth? Are there any abnormalities of the mouth, tongue, palate, or mandible? B, Are any teeth loose or missing? C, Is the mandible of normal configuration? How much space is there between the genu of the mandible and the thyroid cartilage? This space is an indication of the extent of the superior and posterior displacement of the larynx; there should normally be at least one finger breadth in a newborn and three finger breadths in an adolescent.

  • Size of mouth

  • Size of tongue and its relationship to other pharyngeal structures (Mallampati Score)

  • Loose or missing teeth (see Fig. 14.12B )

  • Size and configuration of palate

  • Size and configuration of mandible

  • Location of larynx in relation to the mandible (see Fig. 14.12C )

  • Presence of stridor and, if present:

    • Is stridor predominantly inspiratory, suggesting an upper airway (extrathoracic) lesion (epiglottitis, croup, extrathoracic foreign body)?

    • Is stridor both inspiratory and expiratory, suggesting an intrathoracic lesion (aspirated foreign body, vascular ring, or large esophageal foreign body)? (see )

    • Is the expiratory phase prolonged or stridor predominantly expiratory, suggesting lower airway disease?

  • Baseline oxygen saturation in room air

  • Microtia (underdeveloped pinna): bilateral but not unilateral microtia is associated with difficulty in visualizing the laryngeal inlet (grade 3 or 4 in the Cormack-Lehane classification, see Fig. 14.22 later). Five (42%) of 12 children with bilateral microtia were found to have a difficult laryngeal view compared with 2 (2.5%) of 81 children with unilateral microtia and 0 of 93 children without microtia. Microtia may represent a mild form of hemifacial microsomia and its associated mandibular hypoplasia. The advantage of understanding this association is that ear deformity is often a more easily recognized clinical finding than mandibular hypoplasia.

  • Global appearance: Are there congenital anomalies that may fit a recognizable syndrome? The finding of one anomaly mandates a search for others. If a congenital syndrome is diagnosed, specific anesthetic implications must be considered (see E-Table 14.1 ).

E-TABLE 14.1
Syndromes and Disease Processes With Associated Airway Difficulties
Syndrome Airway Cerebral Cardiac Renal Gastrointestinal Endocrine Metabolic Musculoskeletal Anesthetic Considerations
Achondroplasia Midfacial hypoplasia, small nasal passages and mouth Megacephaly ± hydrocephalus due to narrow foramen magnum Dwarfism; odontoid hypoplasia with atlantoaxial instability DI; difficult mask airway, ± hydrocephalus
Apert syndrome Maxillary hypoplasia, narrow palate ± cleft palate Craniosynostosis, flat facies, hypertelorism ± Congenital heart disease ± Hydronephrosis, ± polycystic kidney ± Esophageal atresia Syndactyly DI; associated cardiac and renal problems
Arthrogryposis multiplex congenita (multiple congenital contractures) Associated hypoplastic mandible, cleft palate, Klippel-Feil syndrome, torticollis ± Ventricular septal defect Thoracolumbar scoliosis DI; associated cardiac disease; minimal muscle relaxant required, ± malignant hyperthermia
Beckwith-Wiedemann syndrome (visceromegaly) Macroglossia: regresses with age; may require partial glossectomy ± Mental handicap due to hypoglycemia Large heart Enlarged kidneys Omphalocele, hepatosplenomegaly Hypoglycemia up to 4 months of age, polycythemia Eventration of diaphragm DI; asymptomatic hypoglycemia; omphalocele; neonatal polycythemia
Cherubism (fibrous dysplasia of jaw) Bilateral painless mandibular and maxillary swelling may progress to airway obstruction DI due to intraoral masses
Congenital hypothyroid Large tongue May be mentally handicapped Hypothermia, hypometabolic Umbilical hernia DI; hypothermia; decreased drug metabolism
Cornelia de Lange syndrome High-arched palate, micrognathia, spurs at anterior angle of mandible, large tongue, ± cleft palate, short neck Mental handicap ± Congenital heart disease DI; associated cardiac disease
Craniofacial dysostosis of Crouzon (Crouzon syndrome) Maxillary hypoplasia with inverted V -shaped palate, ± large tongue Ocular proptosis due to shallow orbits, craniosynostosis DI; eye injury
Epidermolysis bullosa Pressure lesions to mouth and airway Need gentle intubation with small tube; postoperative laryngeal obstruction due to bulla formation
Freeman-Sheldon syndrome (whistling face) Small mouth, high palate Hypertelorism, ± increased intracranial pressure, ± mental deficiency, ± microcephaly Craniocarpotarsal dysplasia; strabismus; kyphoscoliosis; hip/knee contractures DI; ± malignant hyperthermia
Goldenhar syndrome (oculoauriculovertebral syndrome) Hypoplastic zygomatic arch, mandibular hypoplasia, macrostomia, ± cleft tongue, palate, tracheoesophageal fistula Hydrocephalus Occipitalization of atlas, cervical vertebral defects DI; cervical spine defects
Hallermann-Streiff syndrome (oculomandibulodyscephaly) Malar hypoplasia, micrognathia, hypoplasia of rami and anterior displacement of TMJ, narrow high-arched palate DI
Marfan syndrome Narrow facies with narrow palate Dissecting aortic aneurysm, aortic insufficiency Scoliosis, kyphosis DI; associated cardiac and pulmonary disease
Mucopolysaccharidoses
Type IH (Hurler) Coarse facial features, macroglossia, short neck, tonsillar hypertrophy, narrowing of laryngeal inlet and tracheobronchial tree ± Increased intracranial pressure Severe coronary artery and valvular heart disease, cardiomyopathy Hepatosplenomegaly Joint stiffness, kyphosis, contractures, odontoid hypoplasia, and atlantoaxial subluxation DI; cervical spine instability; postobstructive pulmonary edema
Type IH/S (Hurler-Scheie) Macrocephaly, micrognathia Mild mental deficiency to normal intelligence ± Valvular disease ± Hepatosplenomegaly Mild joint stiffness ± DI
Type IS (Sheie) or type V Mandibular prognathism Normal intelligence, corneal clouding Aortic insufficiency Joint stiffness ± DI
Type II (Hunter) Coarse facial features, tracheomalacia, macrocephaly, macroglossia Increased intracranial pressure, severe mental deficiency Valvular heart disease, cardiomyopathy Hepatosplenomegaly Joint stiffness, dwarfism, kyphoscoliosis DI
Type III (Sanfilippo) Mildly coarse facial features Severe mental deficiency ± DI
Type IV (Morquio) Mildly coarse facial features, prominent mandible, short neck Late-onset aortic regurgitation Joint laxity, kyphoscoliosis, odontoid hypoplasia with atlantoaxial instability DI; cervical spine instability; restrictive pulmonary disease
Nager syndrome Micrognathia, cleft palate Low-set ears, atresia of external auditory canal Radial limb defects DI
Papillomatosis larynx and trachea Difficult laryngoscopy Pulmonary hypertension DI; care not to seed papilloma into trachea
Pierre Robin syndrome (Robin sequence) Hypoplastic mandible; pseudomacroglossia; ± high-arched, cleft palate DI
Pompe disease (cardiomuscular glycogen storage disease) Large tongue Cardiomyopathy Muscle weakness DI; muscle weakness, sensitive to muscle relaxants; congestive heart failure, sensitive to myocardial depressants
Rheumatoid arthritis TMJ mobility limited, hypoplastic mandible, cricoarytenoid arthritis with narrow larynx Myocarditis, valvular disease, especially aortic insufficiency Steroid therapy, anemia Cervical spine subluxation, rigid cervical spine DI; cervical spine instability; associated heart disease; problems with positioning; steroid therapy
Rubinstein-Taybi syndrome Maxillary hypoplasia, narrow palate Mental handicap ± Congenital heart disease Associated cervical vertebral anomalies DI; cervical spine instability; associated cardiac disease
Scleroderma Extensive scarring of mouth, face, body Steroid therapy DI; decreased pulmonary compliance; steroid therapy
Smith-Lemli-Opitz syndrome Micrognathia, ± cleft palate, recurrent pneumonia Moderate mental handicap, microcephaly ± Congenital heart disease DI; associated cardiac disease
Stevens-Johnson syndrome Laryngeal, tracheal, bronchial, bullae, pneumothorax, pleural effusion Myocarditis Urethritis Esophagitis, fluid shifts Temperature elevations DI; fluid balance; myocarditis; temperature control; avoid intubation if possible
Thalassemia major (Cooley anemia) Malar hypoplasia causes relative mandibular hypoplasia Hemosiderosis May be DI; anemia; associated cardiac disease
Treacher Collins syndrome Malar, mandibular hypoplasia, ± cleft lip, ± choanal atresia, ± macrostomia or microstomia ± Congenital heart disease ± Cervical spine deformity DI; associated cardiac disease
Trisomy 21 (Down syndrome) Small mouth, hypoplastic mandible, protruding tongue Mental handicap Atrioventricular communis, ventricular septal defect, atrial septal defect Duodenal atresia Hypotonia, cervical spine subluxation May be DI; associated cardiac disease; require less muscle relaxant; increased risk of postintubation stridor
Turner syndrome (Noonan syndrome) Narrow maxilla, small mandible, short neck Mental handicap Coarctation of aorta in females, pulmonary artery coarctation in males Idiopathic hypertension Hypogonadism DI; associated cardiac disease; hypertension
CHD, congenital heart disease; DI, difficult intubation; TMJ, temporomandibular joint; ± , may or may not have the problem.

Diagnostic Testing

Routine evaluation of the airway usually requires only a careful history and physical examination. In the presence of airway pathology, however, laboratory and radiologic evaluation can be extremely valuable. Radiographs of the upper airway (anteroposterior and lateral films and fluoroscopy) may provide evidence about the site and cause of airway obstruction. When necessary, MRI, CT, and three-dimensional (3-D) modeling provide more detailed information. Radiologic airway examination in a child with a compromised airway may be undertaken only if there is no immediate threat to the child's safety and only in the presence of skilled and appropriately equipped personnel able to manage the airway. Securing the airway through tracheal intubation must not be postponed to obtain a radiologic diagnosis when the child has severely compromised air exchange. Blood gas analysis is occasionally of value for assessing the degree of physiologic compromise, especially with chronic airway obstruction and compensated respiratory acidosis. Performing an arterial (or venous) puncture for blood gas analysis may provide helpful information, but it is often upsetting to the child and may risk aggravation of the underlying airway obstruction through dynamic airway collapse. Candidates for blood gas analysis must be carefully selected and the procedure skillfully performed.

Endoscopic evaluation (flexible fiberoptic endoscopy) of the airway before tracheal intubation can be useful in infants and in cooperative older children if a glottic pathologic process is suspected or if difficulty is anticipated when visualizing the glottis. Ultrasound can also be used to examine the airway. It can be used to determine the internal diameter of the trachea, which can help with the selection of the optimal ETT size.

Airway Management: The Normal Airway

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